The authors investigated the usability of ¹²³I-iomazenil SPECT (IMZ-SPECT) in order to identify the possible site of epileptogenic focus in patients of intractable localization-related epilepsies. Prior to IMZ-SPECT, localization of the epileptogenic focus of 25 patients (14 males and 11 females) were investigated by clinical seizure manifestations, EEG figures and neuroimaging including MRI and regional cerebral blood flow (rCBF) SPECT. The clinical diagnosis was: temporal lobe epilepsy in 14 patients, frontal lobe epilepsy in 7 and parietal lobe epilepsy in 2. The location of focus could not definitely determined in 2 patients. Scanning of IMZ-SPECT was conductedin 2 stages; 5-35 min (early image) and 165-195 min (late image) after the injection of ¹²³I-iomazenil. In 23 patients whose focus localization was electroclinically identified, low accumulation area of redioactivity coincident with the site of epile-ptogenic focus was found in 17 patients (74%) in early image and 20 cases (87%) in late image was considered to account for distribution of benzodiazepine receptor. The rate was apparently superior compared to that of MRI (74%) and interictal rCBF SPECT (70%) and almost equivalent to ictal rCBF SPECT (95%). We emphasized that IMZ-SPECT especially its late image is usable as a non-invasive technique for detecting the site of epileptogenic focus in patients with localization-related epilepsies.

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In order to elucidate the pathophysiology of epilepsy with intracranial arachnoid cysts, we studied the relationships between encephalographic findings and the location the volume of arachnoid cysts.
Subjects in this study were thirty-three patients (27 males and 7 females, ranging in age from O month to 13 years (4.0±4.2 years)) with primary intracranial arachnoid cysts. Cases with secondary arachnoid cysts and cases involving arachnoid cystectomy were excluded. Cysts were located in the middle cranial fossa in 21 cases, in the supratentorial location other than the middle cranial fossa in 4 cases, and in the infratentorial area in 8 cases. EEG abnormalities were observed in 21 cases, out of which 11 cases (the epileptic group) exhibited epileptic seizures (partial seizures, 7 cases; generalized seizures, 4 cases). Among the cases of cysts in the infratentrial area, 2 cases showed partial seizures and focal spikes in their EEGs. The volume of arachnoid cysts was significantly larger in the non-epileptic group with EEG abnor-malities than in the epileptic group (p<0.03).
Our study suggests that the epilepsy seen with arachnoid cysts is not directly caused by the cysts perse. Cerebral lesions accompanying arachnoid cysts may partici-pate in the development of epilepsy.

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Psychiatric manifestations following temporal lobectomy in twenty two patients were examined. Three patients experienced de novo psychosis after right temporal lobectomy. Depression occured within three months after the temporal lobectomy and lead to suicide attempt in extreme cases. Preoperative agression and hostility were ameliorated. Although most of the postoperative psychiatric symptoms disappeared within a year following surgery, abnormal mental states continued to be present for more than twelve months in two cases.
The comparison between the group of patients with postoperative abnormal mental states (n=10) and that without (n=12) revealed abundance of ictal fear as well as dreamy state and predominance of the history of presurgical psychotic episode in the former. In view of the postoperative psychosis described in the literature, the current study suggested that postoperative psychiatric manifestations could not be explained fully by the psychogenic theory, and that not only neurological and neuropsy-chological but also psychiatric assessments were essential following temporal lobectomy. Most of the postoperative psychotic episodes could be shortened or aborted by an appropriate medical therapy. Recognition of them as early as possible is all the more important for it.

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We evaluated the efficacy of clonazepam (CZP) treatment for Rolandic discharge (RD) in patients suffering from benign childhood epilepsy with centro-temporal spikes (BCECT). Twenty newly diagnosed patients received CZP twice a day. The dose administered ranged form 0.35 to 1.0mg/day. Both before and one month after the institution of the medication, the EEGs of each patient were evaluated in both the awake and natural sleeping states.
The RD disappeared in the EEG of 15 patients one month after beginning the medication. We also recorded the EEGs in 13 patients one week after starting the medication. In 6 of these 13 patients the RD had already disappeared by that point.
In 12 of 15 patients whose RD disappeared one month after the start of medication, the efficacies of CZP for RD in EEG and for seizures were continuously investigated for from 8 months to 6 years and 8 months. RD appeared again in 10 patients and 6 of these 10 patients had a relapse of seizures.
We thus propose that the immediate efficacy of CZP for RDs be accepted as a new characteristic of the EEG in BCECT. However, long term monotherapy with CZP for BCECT is not necessarily recommended because tolerance to this therapy would be expected to develop in the long run.

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The clinical effects and plasma levels of zonisamide (ZNS) were investigated in children with cryptogenic localization-related epilepsies, who were administered ZNS once a day as a single drug. ZNS is absorbed slowly from the gastrointestinal tract, and its biological half-life is long compared with the other prevalent antiepileptic drugs.
The patients comprised 45 previously untreated children aged 3 months to 14 years (mean, 8 years and 6 months) with any of simple, complex or secondarily generalized partial seizures. A daily dose of 2mg/kg of ZNS was introduced and the dosage was increased gradually to the initial maintenance daily dose of 8mg/kg. ZNS was prescribed once a day in the morning. Blood samples for determination of the plasma levels were taken before and 4 hours after the morning dose, each of which represents the trough and peak levels in a day.
The initial maintenance daily dosage of ZNS (8.01±0.54mg/kg) gave the trough and peak plasma levels of 27.1±8.2 and 33.4±9.1μg/ml, respectively. The peak totrough plasma level ratios were as small as 1.25±0.13. The plasma level (μg/ml) to dose (mg/kg/day) ratios estimated by the trough and peak plasma levels increased both with the advance in age, but the peak to trough plasma level ratios were maintained almost uniformly throughout the pediatric age period.
Of the total 25 patients who were followed up clinically for more than 12 months, seizures were not controlled in 5 with the initial maintenance dosage. Three of the 5 patients who had seizure recurrences showed the trough plasma ZNS levels around 15μg/ml. In 3 patients whose peak levels were above 40μg/ml, the dosage was decreased to tolerable levels because of the continuous complaint of drowsiness.However, for the period of treatment, ranging from 12 to 34 months (mean, 15.7months) from starting ZNS therapy, complete seizure control was obtained in 17 out of the 25 patients on the initial maintenance dosage.
Once-daily dose of ZNS monotherapy assisted by blood level monitoring may be effective for the control of partial seizures in children.

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We report a 12-year-old girl with double cortex syndrome. She was moderately retarded and had bilateral tonic seizures of upper extremities and atonic seizures of lower extremities with consciouness disturbances. An interictal EEG showed two foci of spikes, left frontpolar and left posteriortemporal.
She was hospitalized due to fluctuating disturbance of consciousness from a nearly normal to an almost unresponsive state. An electro-encephalogram recorded during the unresponsive state disclosed a diffuse but posteriorly predominant 4-5 Hz hypersynchronous waves that began as a 10-11 Hz focal rhythmic waves at left parietooccipital or frontal area. 2-3 Hz spike and wave complex, following right frontal dominant 12-13 Hz wave, sometimes accompanied this high voltage wave. This pattern continued for a few minutes and the consciousness returned to a nearly normal state as these waves disappeared. This complex partial status was composed of complex partial seisure for some minutes long and interictal state, in which the consciousness did not return to normal. These states were periodically repeated in a few minutes and were effectivey controlled by intravenous diazepam.
Although double cortex syndrome is a rare migratory disorder, it has often been reported together with intractable epilepsy. As far as we know, this is the first case of double cortex syndrome accompanied by complex partial status epilepticus.

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Aplastic anemia was developed in a woman during carbamazepine (CBZ) monotherapy.She began to be treated with CBZ for complex partial seizures and developed pancytopenia 6 months later. She did not show any of clinical complaint, petechia and signs of infection. Bone marrow examination showed marked hypoplasia, which was diagnosed as aplastic anemia. Lymphocyte stimulating test using CBZ was negative. Discontinuation of CBZ and administation of both predonisolone and anabolic steroid was followed by hematological remission after 4 months. Necessity of routine laboratory monitoring of antiepileptic medication was controversial because of its expensiveness. However, it should be aware of the importance to monitor side effects routinely in patients who are under anticonvulsant therapy, since some of them might have serious illness, such as aplastic anemia, with little of clinical symptoms and signs.

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